We have known for many years that physical activity and adequate nutrition are important for the maintenance of the mass of muscle, tendon and bone in human beings. However the underlying mechanisms are only slowly being relieved partly because human beings often show significant biological differences in the organisation and effectiveness of the control mechanisms, highlighting the need for experimental studies in people. Work from our laboratory and that of colleagues has demonstrated that amino acids are major drivers of anabolism in muscle and bone but that tendon is unresponsive to nutritional influences. The amino acid induced effects in muscle, which appear to be mainly due to their effects on stimulation of protein synthesis are independent of the actions of insulin and growth hormone. Insulin seems to be of major importance in the regulation of protein breakdown in muscle with a very steep dose response relationship between availability of insulin and inhibition of breakdown. Both in muscle and bone amino acids are responsible for rapid alterations in transcription of genes associated with anabolism as well as proteins associated with anabolic signalling pathways. Short term alteration of availability of glucose and lipid have no influence on muscle or bone maintenance (except in the context of insulin secretion) but evidence is growing that polyunsaturated fatty acids may have an anabolic role in muscle. Exercise is anabolic in itself but the ability to increase muscle protein balance depends upon the availability of amino acids. Exercise will stimulate the ability to make protein for up to 48 h after exercise and although it is well understood that different modes of exercise (e.g. resistance vs. endurance) cause stimulation of different suites of genes leading to characteristic muscle adaptation, somewhat surprisingly, any kind of exercise appears to stimulate the propensity for bulk muscle protein synthesis. There are no major differences in the effects of so called “concentric” (shortening) or “eccentric” (lengthening) exercise on the acute increases in muscle protein synthesis although it is known that the latter provides a better stimulus for muscle growth. However the expression of genes associated with muscle building shows dramatic differences between these two modes, which are likely to be important for muscle building. Tendon despite being impervious to alterations of nutrition shows marked increase in collagen synthesis as a result of alteration of activity; this is also true of collagen synthesis in muscle. There is growing evidence that although growth hormone has no effect on muscle myofibrillar and sarcoplasmic synthesis it may markedly stimulate collagen synthesis in muscle and tendon. Ageing and a wide variety of chronic disease processes cause decreases in the ability of muscle to make protein in response to adequate nutrition, a phenomenon which we call anabolic resistance and which appears to have its basis in alterations both in gene transcription and capacity and activity of signalling pathways.